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Published on: January 25, 2016
Paradoxical (REM) sleep genesis by the brainstem is under hypothalamic control.
Pierre-Hervé Luppi1, Olivier Clément, Patrice Fort
1INSERM, U1028, CNRS, UMR5292, Lyon Neuroscience Research Center, Team "Physiopathologie des réseaux neuronaux responsables du cycle veille-sommeil", Lyon, France; University Lyon 1, Lyon, France.
Current Opinion in Neurobiology
|March 16, 2013
Summary
This review hypothesizes that MCH/GABAergic neurons in the lateral hypothalamus initiate and maintain paradoxical (REM) sleep. These neurons inhibit PS-off neurons, which gate PS-on neurons in the SLD, controlling REM sleep features.
Area of Science:
- Neuroscience
- Sleep Science
- Neurophysiology
Background:
- Paradoxical sleep (PS), also known as REM sleep, is a complex brain state.
- Understanding the precise mechanisms governing PS onset and maintenance is crucial for sleep research.
Purpose of the Study:
- To present a novel hypothesis on the neurobiological mechanisms underlying paradoxical (REM) sleep genesis.
- To integrate recent findings into a cohesive model of PS regulation.
Main Methods:
- This is a review article, synthesizing existing research and data.
- The hypothesis is based on the interpretation of current experimental results.
Main Results:
- The proposed model implicates MCH/GABAergic neurons in the lateral hypothalamus as key initiators of PS.
- These neurons are hypothesized to inhibit ventrolateral periaqueductal gray (vlPAG) GABAergic PS-off neurons.
- PS-off neurons are suggested to gate the activation of sublaterodorsal tegmental nucleus (SLD) glutamatergic PS-on neurons, which control REM sleep phenomena like cortical activation and muscle atonia.
Conclusions:
- The hypothesis provides a framework for understanding REM sleep regulation.
- Further research is needed to experimentally validate the proposed roles of these neuronal populations in PS genesis.
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